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电场中细胞突起形成的机制:肌动蛋白的作用。

Mechanism of cell protrusion formation in electrical field: the role of actin.

作者信息

Popov S V, Svitkina T M, Margolis L B, Tsong T Y

机构信息

Department of Biochemistry, University of Minnesota, St. Paul.

出版信息

Biochim Biophys Acta. 1991 Jul 22;1066(2):151-8. doi: 10.1016/0005-2736(91)90181-7.

Abstract

An intense alternating current electrical field that imposes membrane-applied force on the cell surface can induce formation of cell protrusions (Popov, S.V. and Margolis, L.B. (1988) J. Cell Sci. 90, 379-389). This technique has been used to investigate the role of actin in the cell protrusion formation. Platinum replicas of the cytoskeleton were prepared to characterize the organization of the cytoskeleton in external force-induced protrusions. Bundles of microfilaments were found in the processes. A specific inhibitor of actin polymerization, cytochalasin B, as well as inhibitors of ATP synthesis (sodium azide and carbonyl m-chlorophenylhydrazone) did not change the morphology of electrical field-generated protrusions, revealed by scanning electron microscopy. However, organization of the cytoskeleton inside the processes changed drastically using these inhibitors. The results of these experiments demonstrate that (i) Membrane-applied force is sufficient to produce native-like cell protrusions, even in conditions where activity of the cytoskeleton is inhibited; (ii) Actin microfilaments can be organized into bundles directly under the action of membrane-applied force. The significance of these observations to cell protrusion formation under normal physiological conditions is discussed.

摘要

施加于细胞表面的膜作用力的强交变电流电场可诱导细胞突起的形成(波波夫,S.V.和马戈利斯,L.B.(1988年)《细胞科学杂志》90卷,379 - 389页)。该技术已被用于研究肌动蛋白在细胞突起形成中的作用。制备细胞骨架的铂复制品以表征外力诱导突起中细胞骨架的组织。在这些突起中发现了微丝束。肌动蛋白聚合的特异性抑制剂细胞松弛素B以及ATP合成抑制剂(叠氮化钠和间氯苯腙羰基)并未改变电场产生的突起的形态,这通过扫描电子显微镜得以揭示。然而,使用这些抑制剂时,突起内部细胞骨架的组织发生了巨大变化。这些实验结果表明:(i)即使在细胞骨架活性受到抑制的情况下,施加于膜的力足以产生类似天然的细胞突起;(ii)肌动蛋白微丝可在施加于膜的力的直接作用下组织成束。讨论了这些观察结果对正常生理条件下细胞突起形成的意义。

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